Deficiencies in a single gene can cause dramatic effects in brain function and so behavior. Linking the known genetic defect with the observed brain disorder has proven to be challenging. Here we describe experiments to link the neurological properties of mocha mice, its aberrant balance, overanxiety, and sensitivity to anesthetics to its underlying molecular deficiency, the absence of the heterotrimeric adaptor protein nAP-3. We have established already that nAP-3 is required for the formation of synaptic vesicles from endosomes, by a pathway sensitive to brefeldin A and the casein kinase inhibitor CKI-7. We use these pharmacological agents to mimic the mocha phenotype in the neuroendocrine cell line PC12. We ask if the presence of "mocha-like" conditions reveals or induces the expression of a different class of synaptic vesicles. Because secretory granule membranes are recycled to synaptic vesicles by an nAP-3 dependent mechanism, we examine the regulated secretory pathway in "mocha-like" PC12 cells. Finally, we initiate studies on mocha mice to determine if their properties are consistent with the findings from PC12 cells and if they are a valid model for the human disease, Panic Disorder Syndrome, which is a major portal to drug addiction.